Electrophysiological effects of nitric oxide in mouse superior mesenteric ganglion.

Electrophysiological effects of nitric oxide in mouse superior mesenteric ganglion.
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一氧化氮对小鼠肠系膜上神经节的电生理作用。

DOI:
10.1152/ajpgi.1996.270.2.g324
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发表时间:
1996
期刊:
The American journal of physiology.
影响因子:
--
通讯作者:
Szurszewski,JH
Szurszewski,JH
中科院分区:
--
文献类型:
--
作者:
Mazet,B;Miller,SM;Szurszewski,JH

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使用细胞内记录技术在体外研究硝普钠 (SNP) 产生的一氧化氮 (NO) 对小鼠肠系膜上神经节 (SMG) 神经元的影响。 SNP 溶液导致大多数 (64%) 测试的神经元发生膜超极化,或导致 8% 的测试神经元发生超极化,然后去极化。 SNP 诱导的超极化在低 Ca2+ 高 Mg2+ 溶液中持续存在,表明 NO 对突触后膜有直接影响。 SNP 的超极化作用被氧合血红蛋白降低或消除。结肠神经的电刺激在正常克雷布斯溶液中的神经元群体中引起晚期缓慢兴奋性突触后电位(晚期 sEPSP)。在 NG-硝基L-精氨酸(一种 NO 合酶抑制剂)存在下,晚期 sEPSP 的振幅显着增强。结果,特别是用 NO 合酶抑制剂观察到的结果,表明内源性 NO 通过重复的神经刺激在小鼠 SMG 中释放,并且它可能通过对神经节神经元的直接作用来调节缓慢的突触传递。
Effects of nitric oxide (NO) generated from sodium nitroprusside (SNP) on neurons of mouse superior mesenteric ganglion (SMG) were studied in vitro using intracellular recording techniques. SNP solutions caused a membrane hyperpolarization in the majority (64%) of the neurons tested or a hyperpolarization followed by a depolarization in 8% of the neurons tested. The SNP-induced hyperpolarization persisted in a low-Ca2+ high-Mg2+ solution, indicating a direct effect of NO on the postsynaptic membrane. The hyperpolarizing effect of SNP was reduced or abolished by oxyhemoglobin. Electrical stimulation of the colonic nerves evoked a late slow excitatory postsynaptic potential (late sEPSP) in a population of neurons in normal Krebs solution. The amplitude of the late sEPSP was significantly enhanced in the presence of NG-nitroL-arginine, a NO synthase inhibitor. The results, particularly those observed with the NO synthase inhibitor, suggest that endogenous NO was released in the mouse SMG by repetitive nerve stimulation and that it modulated slow synaptic transmission, presumably by a direct action on ganglionic neurons.
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